Both thyroid hormones and glucocorticoids regulate (Na++K+)-adenosine triphosphatas (NaK-ATPase) activity. My overall goal is to elucidate the biochemical mechanisms involved in the processes. In previous studies, I obtained evidence that administration of triiodothyronine (T3) to thyroidectomized rats induces the synthesis of the large and small subunits of this enzyme in rat renal cortex. To reinforce the significance of these findings, one objective is to determine whether T3 also induces amino acids incorporation into this enzyme in rat salivary glands. To do so, thyroidectomized rats, pretreated with T3 or the diluent, will be infused with radiolabeled methionine and incorporation into the subunits will be estimated by DodSO4 polyacrylamide gel electrophoresis. A second objective is to determine whether T3 also induces carbohydrate incorporation into this enzyme in rat salivary glands. So far, induction of the synthesis of both subunits by T3 has been shown only in the rat kidney. To reinforce the general significance of the mechanism of T3 on NaK-ATPase, I plan to study the effect of T3 on NaK-ATPase units in rabbit salivary glands. If T3 induces the synthesis of the subunits of NaK-ATPase in rat salivary glands, in vivo, I plan to examine whether the same mechanisms of action on NaK-ATPase system occurs in primary cultured salivary gland cells. Finally I plan to explore the biochemical basis of the action of glucocorticoids on NaK-ATPase units in rat salivary glands. The time course of the response to a standard amount of glucocorticoids in adrenalectomized rats will be defined in the salivary glands. Glucocorticoid-dependent increases in NaK-ATPase will be compared to effects on NaK-ATPase content by labeling with [gamma-32P)ATP. In addition, I plan to evaluate the role of induction of the synthesis of NaK-ATPase in this process by incorporation of labeled amino acids and SDS-polyacrylamide gel electrophoresis. These studies have a reasonable probability of yielding valuable information on the regulation of Na+ pump activity by thyroid hormones and glucocorticoids.